Article Summary
陆跃武1 耿华云1 张峰1 盖灿1 韩慧杰1 孙海英2.三氧化二砷对K562/A02 细胞的凋亡及细胞周期的影响[J].现代生物医学进展英文版,2012,12(15):2852-2854.
三氧化二砷对K562/A02 细胞的凋亡及细胞周期的影响
Effect of Arsenic Trioxide on Cell Cycle and Apoptosis of MultidrugResistant K562/A02 Cell Line
  
DOI:
中文关键词: 三氧化二砷  多药耐药  K562/A02  细胞凋亡  细胞周期
英文关键词: Arsenic trioxide  Multi-drug resistant  K562/A02  Apoptosis  Cell cycle
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Author NameAffiliation
LU Yue-wu1, GENG Hua-yun1, ZHANG Feng1, GAI Can1, HAN Hui-jie1, SUN Hai-ying2 淮北市人民医院内二科 
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中文摘要:
      目的:研究三氧化二砷对多药耐药急性白血病细胞株K562/A02 凋亡与细胞周期的影响及可能机制。方法:取阿霉素(Adr)的 耐药白血病细胞株分为未加药的对照组及加入不同浓度的三氧化二砷(其终浓度为4.0μmol/L、5.0μmol/L) 组,流式细胞仪检测细 胞凋亡及细胞周期分布, Western blot 方法检测不同浓度三氧化二砷对K562/A02 细胞核NF-κBp65 蛋白水平。结果:与对照组比 较,三氧化二砷可显著增加Adr 对K562/A02 细胞凋亡率,阻滞细胞于G0/G1 期,降低K562/A02 细胞胞核中NF-kB p65 的表达(P 均<0.05)。结论:三氧化二砷可能是通过抑制NF-kB 的胞内活化转位,从而促进K562/A02 细胞凋亡及抑制细胞增殖。
英文摘要:
      Objective: To explore the effect of arsenic trioxide on cell cycle and apoptosis of K562/A02 cells and its possible mechanism. Methods: Adriamycin (Adr) resistant K562/A02 were treated with arsenic trioxide (non-cytotoxic concentration at 4.0μmol/L, 5.0μmol/L) or without arsenic trioxide (control), flow cytometry was used to evaluate apoptosis and cell cycle distribution, and change of the expression level of NF-κBp65 protein in nucleus was detected by western blot. Results: As compared with control arsenic trioxide significantly increased the rate of apoptosis, arrested cells in G0/G1phase and reduced the levels of NF-κBp65 protein in nucleus (allP<0.05). Conclusion: The underlying mechanism for arsenic trioxide to promote apoptosis of K562/A02 and suppress cell proliferation lies in its impact on NF-κBp65 protein expression.
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